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  Kinase-independent requirement of EphB2 receptors in hippocampal synaptic plasticity

Grunwald, I. C., Korte, M., Wolfer, D., Wilkinson, G. A., Unsicker, K., Lipp, H. P., et al. (2001). Kinase-independent requirement of EphB2 receptors in hippocampal synaptic plasticity. Neuron, 32(6), 1027-1040. doi:10.1016/s0896-6273(01)00550-5.

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Genre: Zeitschriftenartikel

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 Urheber:
Grunwald, I. C.1, Autor           
Korte, M.2, Autor           
Wolfer, D., Autor
Wilkinson, G. A.1, Autor           
Unsicker, K., Autor
Lipp, H. P., Autor
Bonhoeffer, Tobias2, Autor           
Klein, Rüdiger1, Autor           
Affiliations:
1Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society, ou_1113546              
2Department: Cellular and Systems Neurobiology / Bonhoeffer, MPI of Neurobiology, Max Planck Society, ou_1113545              

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Schlagwörter: long-term potentiation commissural axons ephrin ligands protein-kinase mutant mice memory ltp depotentiation stimulation activation Neurosciences & Neurology
 Zusammenfassung: During development, Eph receptors mediate the repulsive axon guidance function of ephrins, a family of membrane attached ligands with their own receptorlike signaling potential. In cultured glutamatergic neurons, EphB2 receptors were recently shown to associate with NMDA receptors at synaptic sites and were suggested to play a role in synaptogenesis. Here we show that Eph receptor stimulation in cultured neurons modulates signaling pathways implicated in synaptic plasticity, suggesting cross-talk with NMDA receptor-activated pathways. Mice lacking EphB2 have normal hippocampal synapse morphology, but display defects in synaptic plasticity. In EphB2(-/-) hippocampal slices, protein synthesis-dependent long-term potentiation (LTP) was impaired, and two forms of synaptic depression were completely extinguished. Interestingly, targeted expression of a carboxy-terminally truncated form of EphB2 rescued the EphB2 null phenotype, indicating that EphB2 kinase signaling is not required for these EphB2-mediated functions.

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Sprache(n): eng - English
 Datum: 2001
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
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 Identifikatoren: Anderer: WOS:000172886800010
DOI: 10.1016/s0896-6273(01)00550-5
ISSN: 0896-6273
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Titel: Neuron
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Cambridge, Mass. : Cell Press
Seiten: - Band / Heft: 32 (6) Artikelnummer: - Start- / Endseite: 1027 - 1040 Identifikator: ISSN: 0896-6273
CoNE: https://pure.mpg.de/cone/journals/resource/954925560565